Release of endothelium-derived relaxing factor from human umbilical vessels.

Voorde, Johan Van de; Vanderstichele, Hugo; Leusen, I

doi:10.1161/01.res.60.4.517

Cited by 103 publications

(29 citation statements)

References 19 publications

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“…To our knowledge, EDRF production has not been previously demonstrated in pulmonary and systemic blood vessels immediately after birth. An EDRF is produced in human umbilical vascular endothelial cells stimulated by histamine but not ACh (9).…”

Section: Discussionmentioning

confidence: 92%

Endothelium-Derived Relaxing Factor: Presence in Pulmonary and Systemic Arteries of the Newborn Guinea Pig

Davidson

Eldemerdash

1990

Pediatr Res

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ABSTRACT. Endothelium-derived relaxing factor (EDRF), believed to be nitric oxide or a compound that releases nitric oxide, is a potent vasodilator produced by some arteries in response to acetylcholine (ACh) and bradykinin (BK). ACh and BK are potent dilators of perinatal pulmonary and systemic arteries. The objectives of this study were to determine if EDRF is present in newborn vessels and if EDRF mediates the vasodilator actions of ACh and BK. Arterial rings from newborn guinea pigs, 1 to 3 d old, were obtained from a branch of the main pulmonary artery and the descending aorta for isometric force bioassays. At their optimal resting tension, the rings were preconstricted with phenylephrine lo-' M in KrebsHenseleit solution before adding incremental doses of ACh or BK. If the endothelium was intact, ACh (lo-' M) relaxed pulmonary arteries and aortas (64 f 7%, 72 f 9% relaxation, respectively, mean f SE). ACh-induced relaxation (ACh lo-' M) in the pulmonary artery and aorta, respectively, was significantly (p < 0.05) attenuated by 1 ) endothelial removal (11 f 9%, 28 f 10%) by rubbing the ring lumen; 2) methylene blue, 10" M, (6 f 8%, 7 f 3%) that inhibits EDRF-associated cGMP production in smooth muscle; and 3) methemoglobin, lo-' M, (13 f 9%, 17 f 7%) that binds EDRF. The results for BK were similar to ACh for the pulmonary artery but BK did not relax the aorta. Indomethacin diminished relaxation of the pulmonary artery and aorta to the submaximal dose (lo-' M) of ACh but indomethacin did not effect the relaxation to ACh lo4 M or BK. We conclude that EDRF is produced in the guinea pig pulmonary artery and descending aorta at birth and that EDRF is a mediator of the vasodilator actions of ACh and BK. Vasodilation by ACh may also involve activation of the cyclooxygenase pathway. (Pediatr Res 27: 128-132,1990) Abbreviations EDRF, endothelium-derived relaxing factor ACh, acetylcholine BK, bradykinin EDRF, now believed to be nitric oxide or a compound that releases nitric oxide, was discovered in 1980 when acetycholine was found to relax preconstricted rabbit artery strips in vitro only if the luminal endothelial cell lining was intact (1). Subsequently, EDRF has been identified by bioassay techniques in pulmonary and systemic arteries of many mammalian species and substances other than ACh (e.g. BK and calcium ionophore) have been shown to stimulate EDRF production. Based on a rapidly expanding body of work (2) that followed the discovery of EDRF, certain bioassay criteria have evolved for attributing vasodilatation to EDRF. These include inhibition of vascular relaxation: 1 ) after removal of or injury to luminal endothelium of the blood vessel (1); 2) by pretreatment with methylene blue that inhibits the increase in cGMP in smooth muscle cells associated with EDRF production (3); and 3) by pretreatment with methemoglobin or Hb that binds EDRF (4).EDRF has not previously been described in pulmonary and systemic blood vessels at birth. It is known that ACh (5) and BK are potent dilators of the perinatal pulm...

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Section: Discussionmentioning

confidence: 92%

Endothelium-Derived Relaxing Factor: Presence in Pulmonary and Systemic Arteries of the Newborn Guinea Pig

Davidson

Eldemerdash

1990

Pediatr Res

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“…Hi-receptor stimulation of cul tured endothelial cells of the human umbilical vein in creases intracellular Ca 2+ (28,29). Release of EDRF from human coronary artery (N. Toda et al, unpub lished data) and umbilical blood vessel segments (12) with the intact endothelium stimulated by histamine is detected by a bioassay system. In the present study, in volvement of endothelium-derived NO in the histamine induced relaxation in monkey cerebral arteries was dem onstrated.…”

Section: Discussionmentioning

confidence: 99%

“…Histamine-induced relaxations mediated by EDRF have been reported in human, monkey and rabbit cerebral arteries (7,8); human and monkey coronary arteries (9,10); guinea pig pulmonary arteries (11); human umbilical vessels (12); monkey pulmonary veins (13); and rat aortas (14). The participation of EDRF is postulated from evidence that the relaxation is dependent on the endothelium and is suppressed by treatment with oxyhemoglobin, methylene blue or anti oxidants.…”

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confidence: 99%

High Affinity Binding of Azasetron Hydrochloride to 5-Hydroxytryptamine3 Receptors in the Small Intestine of Rats

Katayama¹,

Asano²,

Haga³

et al. 1997

Japanese Journal of Pharmacology

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-Monkey cerebral artery strips partially contracted with prostaglandin F2a responded to histamine with biphasic patterns of relaxation. The delayed and sustained relaxation was suppressed by cimetidine, whereas the phasic response was abolished by treatment with chlorpheniramine and NG nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor. The inhibition by L-NA was reversed by L-arginine. D-NA was without effect. Endothelium denudation abolished the phasic relaxation. We hypothesized that endothelium-dependent, phasic relaxations caused by histamine are mediated by NO that is released by Hi-receptor stimulation, whereas the sustained relaxation is associated with the activation of H2-receptors in the smooth muscle of monkey cerebral arteries.Keywords: Histamine, Nitric oxide, Endothelium, Hi-receptor subtype, Cerebral artery (monkey)The complexity of vascular responses to histamine is based on its actions on histaminergic receptor subtypes, H1 and H2, in the endothelium and smooth muscle and on the release of chemical mediators, such as endothelium-derived relaxing factor (EDRF) and pros taglandins (PGs), from endothelial and subendothelial tissues (1 6). Histamine-induced relaxations mediated by EDRF have been reported in human, monkey and rabbit cerebral arteries (7, 8); human and monkey coronary arteries (9, 10); guinea pig pulmonary arteries (11); human umbilical vessels (12); monkey pulmonary veins (13); and rat aortas (14). The participation of EDRF is postulated from evidence that the relaxation is dependent on the endothelium and is suppressed by treatment with oxyhemoglobin, methylene blue or anti oxidants. EDRF has been proposed to be nitric oxide (NO) or an unstable S-nitroso compound that releases the NO radical (15, 16). However, endothelium-depend ent relaxations are not always associated with NO or its analog (17, 18).We have reported that endothelium-dependent re laxations caused by histamine in monkey cerebral arter ies are significantly inhibited by methylene blue and chlorpheniramine, suggesting the involvement of the endothelial H1-receptor subtype in the release of EDRF (7). Despite this conclusion, whether NO was actually involved in the response could not be determined. Methylene blue has many actions other than the inhibi tion of soluble guanylate cyclase (19,20), whereas NO synthase inhibitors, including NG-monomethyl-L-argi nine, NG-nitro-L-arginine (L-NA), L-NA methylester, etc. (21), are selective in depressing the synthesis of NO. Thus, the role of NO can be evaluated more speci fically by the use of these inhibitors. In addition, the effectiveness of NO synthase inhibitors on the endo thelium-dependent relaxation has not been evaluated in cerebral arteries.Therefore, the present study was undertaken to eluci date the involvement of endothelium-derived NO in the histamine-induced relaxation of isolated monkey cere bral arteries, with special reference to the histaminergic receptor subtypes. MATERIALS AND METHODS PreparationJapanese monkeys (Macaca fuscata) of eith...

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“…In the case of human umbilical blood vessels, the endothelium releases an EDRF in response to histamine, acting via H, receptors, but not in response to ACh. 21 Thus, it seems that the ability of in vitro vascular preparations to show endotheliummediated effects varies widely with the blood vessel under study. In our study, both ACh and A23187 were effective in relaxing the basilar arteries of five of 11 cases.…”

Section: Discussionmentioning

confidence: 99%

Endothelium-dependent relaxation of human basilar arteries.

Kanamaru

Waga

Fujimoto

et al. 1989

Stroke

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We studied the effects of acetylcholine and calcium ionophore A23187 on human basilar artery rings. Among 11 arteries, both agents produced significant relaxations in five, A23187 but not acetylcholine caused a response in six, and neither agent was effective in four. After rubbing off the endothelium, the relaxations induced by both agents were significantly attenuated. Indomethacin (a cyclooxygenase inhibitor) and AA861 (a specific inhibitor of 5-lipoxygenase) did not but SKF525A (an inhibitor of cytochrome P450-dependent monooxygenase) did significantly inhibit the acetylcholine-induced relaxation in human basilar arteries. On the other hand, AA861 inhibited while neither indomethacin nor SKF525A had any effect on the A23187-induced relaxation. Our results suggest that different mechanisms may be involved in acetylcholine and A23187-induced relaxations in human basilar arteries. (Stroke 1989;20:1208-1211)

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Release of endothelium-derived relaxing factor from human umbilical vessels.

Cited by 103 publications

References 19 publications

Endothelium-Derived Relaxing Factor: Presence in Pulmonary and Systemic Arteries of the Newborn Guinea Pig

Endothelium-Derived Relaxing Factor: Presence in Pulmonary and Systemic Arteries of the Newborn Guinea Pig

High Affinity Binding of Azasetron Hydrochloride to 5-Hydroxytryptamine3 Receptors in the Small Intestine of Rats

Endothelium-dependent relaxation of human basilar arteries.

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